Uric acid is a metabolic product originating from nucleic acids as a carrier of genetic information or ATP as a carrier of energy, and it is secreted as a final degradation product of purine compounds in mammals, etc. Regarding the mechanism of this metabolism, hypoxanthine is converted into xanthine, and then xanthine is converted into uric acid. This reaction is catalyzed by a xanthine oxidase.
When an abnormality in the metabolism of purine compounds by xanthine oxidase occurs, various disorders are caused. As an example, hyperuricemia can be mentioned (Non-Patent Literature 1). In general, saturation solubility of sodium urate in blood serum is believed to be 7 mg/dL at 37° C. Thus, when the blood uric acid concentration is more than 7 mg/dL, there is a possibility that crystals of uric acid are precipitated in a human body. Accordingly, a symptom in which the blood uric acid concentration is more than 7 mg/dL is called “hyperuricemia.” In addition, the abnormality in the metabolism of purine compounds may also cause gout. When the blood uric acid concentration stays continuously high, crystals of uric acid salt accumulate within or around a joint. Due to such phenomenon, a symptom like occurrence of acute arthritis, gouty node, joint dysfunction and joint deformation, etc. is caused. Such symptom is called “gout,” which is a disorder capable of causing various complications like renal dysfunction and vascular dysfunction, etc. In addition, it is known that uric acid is a risk factor for cardiovascular diseases (Non-Patent Literatures 2 to 7) and a cardiovascular disease such as hypertension is caused by the increase in value of uric acid in blood (Non-Patent Literatures 8 to 11).
Conventionally, the number of patients suffering from gout and hyperuricemia is not so high in Japan. As such, not so much attention has been paid to prevention of gout and hyperuricemia. However, in recent years, a rapid change occurs in lifestyle and the number of people who eat high calorie, high protein and high fat foods is on the rise. Furthermore, an increasing number of onset of gout is reported according to increased stress, etc. Thus, greater attention is now being paid to the prevention and amelioration of gout or hyperuricemia, which is a risk factor thereof.
Until now, in order to improve or prevent hyperuricemia, gout, or a cardiovascular disease that is caused by high content value of uric acid in blood, “Probenecid (trade name)” as a uricosuric drug or “Allopurinol (trade name)” as a uric acid-producing inhibitor has been provided. However, those are problematic in that they are transient, and side effects like gastric dysfunction, rash, decrease in white blood cells, decrease in platelets, hepatic dysfunction and renal dysfunction, etc. are accompanied therewith.
As such, in order to prevent or improve the disorders described above, there is a need to control or reduce the value of uric acid in blood to an appropriate level by inhibiting the production of uric acid in a living body.